OBJECTIVE: To evaluate the prevalence of idiopathic hirsutism in a large population of hirsute women. DESIGN: 588 hirsute women (mean age 24+/-1, range 15-36 years) were evaluated as outpatients at the Department of Endocrinology of the University of Palermo, Italy. The diagnosis of idiopathic hirsutism was established in hirsute patients presenting regular ovulatory menstrual cycles and normal serum androgen levels (total testosterone, unbound testosterone and dehydroepiandrosterone sulfate). METHODS: Hirsutism was calculated by the Ferriman-Gallwey-Lorenzo index. Serum androgens were evaluated in the follicular phase (days 5 or 6) and normal androgen ranges were calculated as the mean+/-2S.D. of serum levels of 30 ovulatory non-hirsute women. The presence of ovulation was determined by serum progesterone levels during the presumed luteal phase (days 21 or 22). All steroids were determined by specific RIAs. RESULTS: 36 hirsute women (6%) had regular ovulatory cycles and normal androgen levels and were diagnosed as being affected by idiopathic hirsutism. CONCLUSIONS: Idiopathic hirsutism is a relatively uncommon cause of hirsutism, affecting approximately 6%, of our population.
E. Carmina, R. Lo Coco, P. Lanzara and A. Jannì
In 11 untreated acromegalic patients the plasma GH levels were determined after the acute administration of bromocriptine, haloperidol, pimozide (only in 8 patients) and of placebo. A 50 % or more suppression of the basal GH levels was arbitrarily defined as a positive response. Six patients displayed a positive response to bromocriptine. Five patients displayed a negative response to bromocriptine. Of these, 4 responded to both antidopaminergic drugs.
We conclude that the acute administration of antidopaminergic drugs reduces the GH secretion in some bromocriptine-insensitive acromegalic patients. Therapeutical implications will require further studies.
E Carmina, E Guastella, R A Longo, G B Rini and R A Lobo
Muscle mass plays an important role in determining cardiovascular and metabolic risks in polycystic ovary syndrome (PCOS). In addition, whether lean mass influences carotid intima-media thickness (IMT) in PCOS has not been assessed.
Ninety-five women with PCOS were age- and weight-matched to 90 ovulatory controls. All women had dual X-ray absorptiometry for lean, fat and bone mass, and bone mass density (BMD). Serum testosterone, sex hormone-binding globulin, insulin, and glucose and carotid IMT were determined. Free androgen index (FAI) and insulin resistance (by QUICKI) were calculated.
In PCOS, waist circumference and insulin were higher and QUICKI lower than in controls (P<0.01). Trunk fat mass, % trunk fat, and lean mass were higher in PCOS compared to controls (P<0.01), while total bone mass and BMD were similar. IMT was increased in PCOS (P<0.01) but only 15% of PCOS patients had abnormal (≥0.9 mm) values. Lean mass correlated with fat parameters, insulin, QUICKI, and FAI, but not with total testosterone; and after adjustments for insulin and QUICKI, lean mass still correlated with fat mass (P<0.01) but not FAI. Lean mass correlated with IMT (P<0.01), but this was dependent on insulin. However, excluding those patients with abnormal IMT values, IMT correlated with lean mass independently of insulin. Bone mass correlated with lean and fat mass, but not with insulin or androgen. PCOS patients with ‘pathological’ IMT values had higher % trunk fat, lean mass, and insulin, lower QUICKI, and higher testosterone and FAI compared with those with normal IMT.
Lean mass is increased in PCOS, while bone mass is similar to that of matched controls. The major correlates of lean mass are fat mass and insulin but not androgen. Lean mass also correlated with IMT, and although influenced by insulin, small changes in IMT may partially reflect changes in muscle mass, while clearly abnormal values relate to more severe abnormalities of PCOS.
E Carmina, N Napoli, R A Longo, G B Rini and R A Lobo
Objective: Metabolic syndrome (MBS) is a common disorder and is thought to be extremely prevalent in polycystic ovary syndrome (PCOS). In the USA the prevalence of MBS in PCOS has been reported to be as high as 43–46% using Adult Treatment Panel III (ATP-III) criteria. Because of differences in diet, lifestyle and genetic factors, we postulated that the prevalence of MBS might not be as high in Italian women. This study sought to determine the prevalence of MBS in Italian women using both the ATP-III and the World Health Organization (WHO) criteria and to determine whether the prevalence is influenced by the way in which PCOS is diagnosed.
Design: Assessment of the prevalence of MBS in 282 women with PCOS, aged 18–40 years, living in western Sicily. Eighty-five age- and weight-matched normal women served as controls.
Methods: Patients were divided into those with chronic anovulation and hyperandrogenism (classic PCOS; n = 225) and others with hyperandrogenism and polycystic ovaries but who were ovulatory (ovulatory PCOS; n = 57). A 75 g oral glucose tolerance test was carried out, as were lipid determinations; insulin resistance was assessed by the Quantitative Insulin-Sensitivity Check Index (QUICKI). We used ATP-III and WHO criteria to diagnose MBS.
Results: Using ATP-III criteria, the prevalence of MBS was 8.2% and using WHO criteria it was 16% in Italian women with PCOS. In controls, the prevalence was 2.4% using both methods. In classic PCOS patients, MBS was higher (8.9% by ATP-III, 17.3% by WHO) than in ovulatory PCOS (5% and 10.6% respectively). Body weight significantly modified prevalence rates.
Conclusion: MBS is substantially higher in women with PCOS than in the general population, and the prevalence is higher in those women diagnosed by classic criteria. However, the prevalence of MBS in PCOS appears to be much lower in Italy than in the USA.
E Carmina, F Orio, S Palomba, T Cascella, R A Longo, A M Colao, G Lombardi and R A Lobo
Background: Adipocytokines are produced by adipose tissue and have been thought to be related to insulin resistance and other health consequences. We measured leptin, adiponectin, and resistin simultaneously in women with polycystic ovary syndrome (PCOS) and age- and weight-matched controls. Our hypothesis was that these simultaneous measurements would help determine whether adipocytokine secretion is abnormal in PCOS independent of body mass and whether these levels are related to insulin resistance as well as other hormonal changes.
Methods: Fifty-two women with PCOS and 45 normal ovulatory women who were age- and weight-matched were studied. Blood was obtained for adipocytokines (leptin, adiponectin, and resistin) as well as hormonal parameters and markers of insulin resistance as assessed by the quantitative insulin-sensitivity check index. Body mass index (BMI) was stratified into obese, overweight, and normal subgroups for comparisons between PCOS and controls.
Results: Adiponectin was lower (P < 0.05) and resistin was higher (P < 0.05) while leptin was similar to matched controls. Breakdown of the groups into subgroups showed a strong body mass relationship for leptin with no changes in resistin although adiponectin was lower in PCOS, even controlling for BMI. In controls, leptin and adiponectin and leptin and resistin correlated (P < 0.05) but not in PCOS. In controls, all adipocytokines correlated with markers of insulin resistance but not in PCOS.
Conclusions: When matched for BMI status, decreased adiponectin in PCOS represent the most marked change. This alteration may be the result of altered adipose tissue distribution and function in PCOS but no correlation with insulin resistance was found.